Effect of Insulin on Acetylcholine-Induced Vasodilation in Normotensive Subjects and Patients With Essential Hypertension

摘要: Background The present study was designed to directly test the vasodilation action of insulin and its relation endothelium-dependent mechanisms. Methods Results In 18 normotensive subjects 27 patients with untreated mild moderate essential hypertension, we studied effect intrabrachial on changes in forearm blood flow (strain-gauge plethysmography) induced by acetylcholine (at doses 0.15, 0.45, 1.5, 4.5, 15 μg · min−1 dL−1), an vasodilator, or sodium nitroprusside 1, 2, 4 endothelium-independent vasodilator. Local hyperinsulinemia (deep venous plasma insulin, 48±6 51±5 μU/mL control hypertensive patients, respectively) did not affect basal stimulated glucose extraction (control subjects, 3±1% 11±2%, P <.001; 6±1%, <.01 for between-group difference). both significantly potentiated acetylcholine-induced vasodilation, whereas it alter vasodilatory response nitroprusside. N G-monomethyl-l-arginine, inhibitor endothelial nitric oxide synthesis, blunted insulin-induced facilitation but subjects. contrast, potentiation vascular local abolished ouabain, Na+-K+ pump. Conclusions healthy humans alike, physiological per se does increase potentiates regardless metabolic resistance. This is because seen related l-arginine–nitric pathway smooth muscle cell hyperpolarization patients.